Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Permeability”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed1997

Luminal bacteria and small-intestinal permeability.

BACKGROUND: The influence of luminal bacteria on small-intestinal permeability has not been fully assessed. This study addressed this issue. METHODS: Thirty-four subjects (mean age 64 years; range 22-95 years) were investigated for possible small-intestinal bacterial overgrowth (SIBO) with culture of a small-intestinal aspirate. A lactulose/mannitol small-intestinal permeability test was performed, small-intestinal histology assessed and serum vitamin B12 concentrations measured in all subjects. Permeability was also assessed in a control group of 34 asymptomatic volunteers. RESULTS: Urinary lactulose/mannitol ratios were significantly increased in subjects with SIBO with colonic-type flora (P < 0.0005), even in the absence of villous atrophy. Urinary lactulose/mannitol ratios were increased in this group due to significantly increased urinary lactulose concentrations (P < 0.0005) rather than reduced urinary mannitol levels, after correcting for inter-subject variations in renal function. Counts of intraepithelial lymphocytes of CD8 phenotype were significantly increased in this group (P = 0.003). Although a significant correlation was found between intraepithelial lymphocyte counts and small-intestinal permeability overall (P < 0.002), these counts were not significantly different in subjects with SIBO with colonic-type flora whose permeability values were < or = > 0.028, the upper limit of normal in asymptomatic controls. Serum vitamin B12 concentrations did not differ significantly between groups (P > 0.5). Ageing did not independently influence small-intestinal permeability (P > 0.5). CONCLUSIONS: Small-intestinal permeability is increased in subjects with SIBO with colonic-type bacteria. This effect is independent of ageing and not mediated by vitamin B12 deficiency. Although counts of intraepithelial lymphocytes of CD8 phenotype are increased in this disorder, it is also unlikely that these cells play an important causative role in this process. Routine light microscopic assessment underestimates the prevalence of small-intestinal functional disturbance in this disorder.

Bacterial Infections↗
PubMed1994

Quantitative laser scanning confocal microscopy on single capillaries: permeability measurement.

OBJECTIVE: We tested the hypothesis that there is significant solute loss to the superfusate during microvessel solute permeability measurement in frog mesentery which leads to underestimation of permeability coefficient. This is the first application of laser-scanning confocal microscopy to measure microvessel permeability. METHODS: Microvessel permeability to sodium fluorescein (0.5 mg/ml, MW 376) was measured in the presence of bovine serum albumin (10 mg/ml) in Ringer's solution. Every 11-12s an optical section transverse to the vessel axis (x-z section) was collected. The images were corrected for fluorescence attenuation in the z direction and nonuniformity of light collection (shading) in the x direction by comparison to a fluorescent standard. Extravascular fluorescence, which increased linearly with time, and the step increase in fluorescence intensity of the vessel lumen were used to calculate an apparent permeability. Measurements were made first with the tissue superfused with Ringer and second after changing the superfusate to mineral oil in order to retain solute potentially lost to Ringer superfusate. RESULTS: The permeability to fluorescein measured with Ringer superfusate (5.0 +/- SD 2.6 x 10(-5) cm/s; n = 3) was not different from that measured with mineral oil covering the upper mesothelial surface (4.5 +/- 1.9). CONCLUSIONS: Therefore, the loss of sodium fluorescein through the upper mesothelium does not significantly alter permeability under these conditions. These techniques enable detailed analysis of solute concentration gradients surrounding microvessels.

Animals↗
PubMed1990

Capillary permeability factor secreted by malignant brain tumor. Role in peritumoral brain edema and possible mechanism for anti-edema effect of glucocorticoids.

Conditioned media from two human malignant gliomas, C6 rat glioma, Walker 256 carcinosarcoma, and normal human glia were concentrated 50-fold to create a culture supernatant (SUP-C). The effect of SUP-C on rat brain capillary permeability was investigated by measuring the entry of 14C-aminoisobutyric acid (14C-AIB) by means of quantitative autoradiography. The SUP-C contained proteins with a molecular weight of 10 kD or greater. The SUP-C from all tumor cells markedly increased brain capillary permeability, indicating the presence of a permeability factor, whereas that from normal glial cells did not. Glioma cells produced more factor after incubation for 20 hours than 4 hours. The activity of capillary permeability factor in the SUP-C was inhibited by pretreatment of animals with BW755C (lipoxygenase inhibitor), but not with indomethacin (cyclo-oxygenase inhibitor). Pretreatment of animals with dexamethasone prior to intracerebral infusion of tumor SUP-C significantly reduced the factor-induced increase in capillary permeability. On the other hand, coincubating glioma cells with dexamethasone produced SUP-C with a permeability activity that was about one and a half times greater than that without dexamethasone. These results indicate that glucocorticoids produce their anti-edema effects by directly acting on capillary endothelial cells, possibly through the inhibition of phospholipase A2 activity, resulting in a decrease of lipoxygenase rather than cyclo-oxygenase products. The production of capillary permeability factor by tumor cells was not inhibited, but rather enhanced, by administration of glucocorticoids.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed2003

Proteinase-activated receptor-2-induced colonic inflammation in mice: possible involvement of afferent neurons, nitric oxide, and paracellular permeability.

Activation of colonic proteinase-activated receptor-2 (PAR-2) provokes colonic inflammation and increases mucosal permeability in mice. The mechanism of inflammation is under debate and could be neurogenic and/or the consequence of tight-junction opening with passage of exogenous pathogens into the lamina propria. The present study aimed to further characterize the inflammatory effect of PAR-2 activation by investigating: 1) the role of NO, 2) the role of afferent neurons, and 3) a possible cause and effect relationship between colonic paracellular permeability changes and mucosal inflammation. Thus, intracolonic infusion to mice of the PAR-2-activating peptide, SLIGRL, increased both myeloperoxidase (MPO) activity and damage scores indicating colonic inflammation, and enhanced colonic permeability to (51)Cr-EDTA from 2 to 4 h after its infusion. NO synthase inhibitors, L-NAME and aminoguanidine, as well as the neurotoxin capsaicin and NK1, calcitonin gene-related peptide (CGRP) receptor antagonists, SR140333 and CGRP(8-37), prevented SLIGRL-induced MPO and damage score increases and permeability. In contrast, although the tight-junction blocker, 2,4,6-triaminopyrimidine, and the myosin L chain kinase inhibitor, ML-7, prevented SLIGRL-induced increase in permeability, they did not prevent MPO and damage score increases. Taken together our data show that both NO and capsaicin-sensitive afferent neurons are involved in PAR-2-mediated colonic inflammation and paracellular permeability increase. Nevertheless, the inflammation process is not a consequence of increased permeability which results at least in part from the activation of myosin L chain kinase.

Administration, Rectal↗
PubMed1999

Induction of endothelial monolayer permeability by phosphatidate.

Released into the vasculature from disrupted cells or transported to the surface of adjacent effectors, phosphatidate and related lipids may potentiate endothelial cell activation. However, the effect of these lipids on endothelial monolayer barrier integrity has not been reported. The present study documents the induction of endothelial monolayer permeability by phosphatidate. Both long (di-C18:1) and medium (di-C10; di-C8) chain length phosphatidates increased permeability of bovine pulmonary artery endothelial cell monolayers assessed using a well characterized assay system in vitro. Barrier disruption effected by dioctanoyl (di-C8) phosphatidate was markedly potentiated by the addition of propranolol, an inhibitor of endothelial cell "ecto"-phosphatidate phosphohydrolase (PAP), a lipid phosphate phosphohydrolase (LPP) that efficiently hydrolyzes extracellular substrate. Disruption of barrier function by phosphatidate did not result from its non-specific detergent characteristics, since a non-hydrolyzable but biologically inactive phosphonate analog of dioctanoyl phosphatidate, which retains the detergent characteristics of phosphatidate, did not induce permeability changes. Furthermore, neither diacylglycerol nor lyso-PA effected significant increases in monolayer permeability, indicating the observed response was due to phosphatidate rather than one of its metabolites. Phosphatidate-induced permeability was attenuated by preincubation of endothelial cells with the tyrosine kinase inhibitor, herbimycin A (10 microg/ml), and enhanced by the tyrosine phosphatase inhibitor, vanadate (100 microM), implicating a role for activation of intracellular tyrosine kinases in the response. In addition, phosphatidate increased the levels of intracellular free Ca(2+) in endothelial cells and ligated specific binding sites on endothelial cell plasma membranes, consistent with the presence of a phosphatidate receptor. Since phosphatidate generated within the plasma membrane of adherent effectors potentially interacts with endothelial membranes, we evaluated the influence of phosphatidate-enriched neutrophil plasma membranes on endothelial monolayer integrity. The effects of ectopic phosphatidate on endothelial monolayer permeability were mimicked by phosphatidate confined to neutrophil plasma membranes. We conclude that phosphatidate may be a physiologic modulator of endothelial monolayer permeability that exerts its effects by activating a receptor-linked, tyrosine kinase-dependent process which results in mobilization of intracellular stored Ca(2+)and consequent metabolic activation.

Animals↗
PubMed1998

Permeability of lichen planus lesions and healthy buccal mucosa to water.

The resurgence of interest in the oral mucosa as a route for drug delivery requires a thorough understanding of the permeability of this tissue in health and disease. Previous work has indicated that non-keratinized oral mucosa is more permeable than its keratinized counterpart. It has been suggested that pathological hyperkeratotic mucosa, which was previously non-keratinized, would be more permeable than healthy tissue. Equivocal results obtained from animal studies in which chemical or mechanical irritation was used to induce a hyperplastic and hyperkeratotic epithelium, prompted us to conduct a study on the comparison of the permeability to water of lichen planus lesions and healthy buccal mucosa. Buccal mucosa was obtained from six patients with previously confirmed lichen planus and from six clinically healthy patients. Thawed biopsies from each specimen were mounted in flow-through diffusion cells and their permeability to tritiated water determined using a continuous flow-through perfusion system. Specimens were examined histologically before and after permeability experiments. No statistically significant differences between mean steady state flux values (10-20 h) for lichen planus tissue and healthy buccal mucosa were found. These results warrant further studies with other oral conditions associated with hyperkeratosis to establish whether the nature and course of the condition are determinants for the retention or loss of the epithelium's permeability characteristics.

Adult↗
PubMed1999

Repeated measurement of intestinal permeability as an assessment of colitis severity in HLA-B27 transgenic rats.

We report on the development of a method for repeated monitoring of mucosal permeability that allows assessment of the severity of colitis and evaluation of treatment efficacy in HLA-B27 transgenic rats. We determined the extent to which intestinal permeability related to stool condition, colon weight, and histological pathology in precolitic and diseased rats up to 29 weeks old. Intestinal permeability was measured by the urinary excretion of iodixanol at 24 h after oral administration. Mean permeability values increased significantly with age in HLA-B27 rats but remained decreased in the background strain Fischer-344 (F-344) control animals. Macroscopic evaluation of HLA-B27 rat colons between 20 and 24 weeks old showed colonic thickening with colonic wet weights increased from 3.4+/-0.13 mg/kg b.wt. in F-344 rats to 6.79+/-0.73 mg/kg b.wt. (p<.05) in HLA-B27 rats. Histological examination of HLA-B27 rat colons confirmed the colonic inflammation as a chronic active mononuclear cell infiltrate. The increase in colon weight was associated with an increase in permeability: 1.16+/-0.17 mg iodixanol versus 5.37+/-1.3 mg of iodixanol in F-344 and HLA-B27 rats, respectively. Three weeks treatment of HLA-B27 rats with cyclosporin A, but not sulfasalazine, showed a dose-dependent decrease in mucosal permeability and colon weight. Neither treatment improved stool condition. We conclude that the measurement of intestinal permeability by iodixanol excretion is a useful biochemical marker that is associated with increases in colonic weight and histological evaluation of inflammation. These data indicate that this technique may be valuable for diagnostic and evaluation purposes in preclinical models of inflammatory bowel disease.

Animals↗
PubMed1999

Isolated hepatic perfusion for lapine liver metastases: impact of hyperthermia on permeability of tumor neovasculature.

BACKGROUND: Hyperthermic isolated hepatic perfusion (IHP) has been shown to cause significant regression of advanced unresectable liver metastases in patients. Although there are different agents and treatment modalities used in IHP, the contribution of perfusion hyperthermia is unknown. PURPOSE: A large animal model of unresectable liver metastases and a technical standard for IHP in this model were established. This model was used to assess the effects of hyperthermia on vascular permeability of tumors and normal liver tissue during IHP. METHODS: Sixty-five New Zealand White rabbits were used in a series of experiments. Disseminated liver tumors were established by direct injection of 1 x 10(6) VX-2 cells into the portal vein by laparotomy in anesthetized animals. Several surgical perfusion techniques were explored to determine a reliable and reproducible IHP model. Vascular permeability in tumor versus liver was then assessed with Evan's Blue labeled bovine albumin under normothermic (tissue temperature 36.5 degrees C +/- 0.5 degree C), moderate hyperthermic (39 degrees C +/- 0.5 degree C), or severe hyperthermic (41 degrees C +/- 0.5 degree C) conditions. RESULTS: Tumor model and perfusion techniques were successfully established with inflow through the portal vein and outflow through an isolated segment of the inferior vena cava. A gravity driven perfusion circuit with stable perfusion parameters and complete vascular isolation was used. Vascular permeability was higher in tumor than in normal tissues (P = .03) at all time points during IHP. Hyperthermia resulted in a significant (up to 5-fold) increase in permeability of neovasculature; when severe hyperthermia was used, tumor vascular permeability was increased even more than normal liver permeability (P = .01). CONCLUSIONS: The VX-2/New Zealand White rabbit system can be used as a reproducible large-animal model for IHP of unresectable liver metastases. It can be used to characterize the contribution and mechanism of action of different treatment parameters used in IHP. Hyperthermia preferentially increases vascular permeability in tumors compared with liver tissue in a dose-dependent fashion, thus providing a mechanism for its presumed benefit during isolated organ perfusion.

Animals↗
PubMed2000

Inhibition of aquaporin-1 water permeability by tetraethylammonium: involvement of the loop E pore region.

Previously, the only known blockers of water permeability through aquaporin-1 (AQP1) water channels were mercurial reagents such as HgCl(2). For AQP1, inhibition by mercury has been attributed to the formation of a mercaptide bond with cysteine residue 189 found in the putative pore-forming region loop E. Here we show that the nonmercurial compound, tetraethylammonium (TEA) chloride, reduces the water permeability of human AQP1 channels expressed in Xenopus oocytes. After preincubation of the oocytes for 15 min with 100 microM TEA, AQP1 water permeability was reduced by 20 to 40%, a degree of partial block similar to that obtained with 15 min of incubation in 100 microM HgCl(2). The reduction of water permeability was dose-dependent for tested concentrations up to 10 mM TEA. TEA blocks the Shaker potassium channel by interacting with a tyrosine residue in the outer pore region. We tested whether an analogous tyrosine residue in loop E of AQP1 could be involved in the binding of TEA. Using polymerase chain reaction, tyrosine 186 in AQP1, selected for its proximity to the mercury-binding site, was mutated to phenylalanine (Y186F), alanine (Y186A), or asparagine (Y186N). Oocyte expression of the mutant AQP1 channels showed that the water permeability of Y186F was equivalent to that of wild-type AQP1; the other mutant channels did not conduct water. However, in contrast to wild-type AQP1, the water permeability of Y186F was not reduced with 100 microM TEA. These results suggest that TEA reduces AQP1 water permeability by interacting with loop E.

Animals↗
PubMed2000

A new direct test of bladder permeability.

PURPOSE: A proposed cause of interstitial cystitis is increased bladder permeability but to our knowledge this theory has not been proved by direct testing. We developed a safe, relatively painless, direct test of bladder permeability. MATERIALS AND METHODS: The original permeability test involved placing 4% lactulose and 1% rhamnose intravesically, then drawing blood to assay for these sugars. Initial feasibility studies were performed in rabbits with bladder epithelium that was intact or disrupted by a 50% acetone rinse. In humans the initial goal was to distinguish intact bladders from those known to have increased permeability. Since distention is known to increase permeability temporarily, we studied patients with interstitial cystitis immediately after distention. RESULTS: Neither sugar was absorbed from intact rabbit bladders, while each was absorbed from acetone rinsed bladders at 10, 20 and 30 minutes. We used 100 ml. of solution in the initial 8 humans, including 6 with interstitial cystitis and 2 controls. At 30 minutes each sugar was absorbed from interstitial cystitis bladders but neither was absorbed from intact bladders. The test solution was then changed to 5% rhamnose. Mean rhamnose absorption plus or minus standard deviation was much greater in the 6 patients with interstitial cystitis than in 8 controls (26.3 + or - 26.1 versus 0.78 + or - 0.87 nmol. /ml. serum, p = 0.008). With 1 exception interstitial cystitis serum levels were at least 4-fold higher than the highest control level. CONCLUSIONS: This new permeability test clearly distinguishes intact versus distended bladders. It may be performed to test whether bladder permeability is increased in interstitial cystitis.

Animals↗
PubMed2001

Age-related changes in skin permeability of hydrophilic and lipophilic compounds in rats.

The effect of age on intact and stripped skin permeability of lipophilic (ketoprofen and isosorbide dinitrate) and hydrophilic permeants (deuterium oxide and diclofenac sodium) was investigated using STD: Wistar male rats aged 5 to 180 days. The permeability of permeants through intact skin increased with increasing lipophilicity of the permeants at each age, indicating that the permselective property of rat skin is revealed even at 5-days-old. The permeability coefficients through intact skin decreased with increasing age, and the extent of these decreases was higher for lipophilic permeants than that for hydrophilic permeants. On the other hand, the stripped skin permeability of permeants was almost the same at each age, and with aging each permeability coefficient through stripped skin decreased up to 21 days, dramatically during 21-90 days and then gradually again to 180 days. The thickness of the stratum corneum and stripped skin increased according to age with faster growth during 21-90 days. The reciprocal of the mean thickness of stratum corneum and stripped skin correlated well with intact skin and stripped skin permeability (r > 0.9), respectively. These results clarified that the permselectivity of rat skin against lipophilicity of permeant exists at the latest from 5 days after birth. In addition, it is speculated that the thickness of skin is a large factor in the decrease of its permeability with age.

Aging↗
PubMed2001

Intestinal permeability tests in coeliac disease.

Intestinal permeability tests have been used to screen for a wide range of small intestinal diseases, including coeliac disease and enteric infections. Several probe molecules have been used to investigate intestinal permeability including monosaccharides, disaccharides, 51Cr-EDTA and polyethyleneglycol. While many factors may affect intestinal permeability tests, the use of two probe molecules, for example, lactulose and mannitol, and the expression of the result as a ratio minimises the effects of these extraneous factors. Rendering the test solution hyperosmolar was also found to increase the sensitivity of the test in detecting coeliac disease. Intestinal permeability is characteristically elevated in untreated coeliac disease, with a sensitivity of up to 96% for the dual sugar techniques. The reason for this is a consistent increase in the absorption of lactulose (via the paracellular route) due to increased "leakiness" of the intestine and a reduction in the absorption of mannitol (via the transcellular route) due to a reduction in surface area as a result of villous atrophy. The intestinal permeability test allows subjects to be selected for jejunal biopsy in whom the clinical features are compatible with coeliac disease and in timing a follow-up biopsy. It has been postulated that raised intestinal permeability may be involved in the pathogenesis of coeliac disease. Recently, serum measurements of the probe molecules may have a valuable role, particularly in paediatric patients. Sucrose permeability has also been proposed as an accurate marker of adult coeliac disease and shows promise as a noninvasive test.

Celiac Disease↗
PubMed2001

Compound mixtures in Caco-2 cell permeability screens as a means to increase screening capacity.

The purpose of this investigation was a study of simultaneous permeability measurement using compound mixtures (cassette dosing) as an alternative to single compound evaluation in order to increase the capacity of screens for intestinal drug permeability. Drug transport across Caco-2 monolayers was studied, both in the apical to basolateral and the basolateral to apical direction. The apparent permeability coefficients for ten compounds displaying different intestinal transport mechanisms were determined, first as single compounds and then as components of a mixture. Seven beta-adrenoceptor antagonists and baclofen were analysed simultaneously using reversed phase HPLC with UV detection, D-glucose and mannitol were measured by scintillation counting. The results indicated that the Papp from the mixture as donor phase correlated well with that of the single compounds and merely small changes in the Papp of each compound were observed between the single compound and mixture experiments. This minor variation resulted in a change in rank-order of the poorly permeable compounds in the mixture, however, without affecting their association with the permeability class according to the biopharmaceutics classification system (BCS). It can be concluded that the use of compound mixtures is a suitable method for improving the capacity in permeability screens. Further improvement of the throughput may be expected upon automatisation of permeability measurements using robotics combined with increased selectivity using LC-MS analysis.

Adrenergic beta-Antagonists↗
PubMed2001

Co-administration of the health food supplement, bovine colostrum, reduces the acute non-steroidal anti-inflammatory drug-induced increase in intestinal permeability.

Non-steroidal anti-inflammatory drugs (NSAIDs) are effective analgesics but cause gastrointestinal injury. Present prophylactic measures are suboptimal and novel therapies are required. Bovine colostrum is a cheap, readily available source of growth factors, which reduces gastrointestinal injury in rats and mice. We therefore examined whether spray-dried, defatted colostrum could reduce the rise in gut permeability (a non-invasive marker of intestinal injury) caused by NSAIDs in volunteers and patients taking NSAIDs for clinical reasons. Healthy male volunteers (n=7) participated in a randomized crossover trial comparing changes in gut permeability (lactulose/rhamnose ratios) before and after 5 days of 50 mg of indomethacin three times daily (tds) per oral with colostrum (125 ml, tds) or whey protein (control) co-administration. A second study examined the effect of colostral and control solutions (125 ml, tds for 7 days) on gut permeability in patients (n=15) taking a substantial, regular dose of an NSAID for clinical reasons. For both studies, there was a 2 week washout period between treatment arms. In volunteers, indomethacin caused a 3-fold increase in gut permeability in the control arm (lactulose/rhamnose ratio 0.36+/-0.07 prior to indomethacin and 1.17+/-0.25 on day 5, P<0.01), whereas no significant increase in permeability was seen when colostrum was co-administered. In patients taking long-term NSAID treatment, initial permeability ratios were low (0.13+/-0.02), despite continuing on the drug, and permeability was not influenced by co-administration of test solutions. These studies provide preliminary evidence that bovine colostrum, which is already currently available as an over-the-counter preparation, may provide a novel approach to the prevention of NSAID-induced gastrointestinal damage in humans.

Adult↗
PubMed2003

[Vasopressin-dependent water permeability of the basolateral membrane of the kidney outer medullary collecting duct in postnatal ontogenesis in rats].

Kidneys of new-born animals are resistant to arginine vasopressin (AVP). The ability of the hormone to regulate water permeability of the collecting duct can be seen from weaning period, probably due to the maturation of the intracellular signaling pathway. The purpose of the present work was to investigate the effect of V2 receptor agonist dDAVP on the water permeability of OMCD basolateral membrane in 10-, 22- and 60-day old Wistar rats. We also estimated ontogenetic gene expression of AQP2, AQP3, AQP4 and V2 receptor. Osmotic water permeability (Pf) of the basolateral membrane of microdissected OMCD was measured under control conditions and after incubation with the agonist V2 receptor desmopressin (dDAVP; 10(-7) M). Water permeability in 10- and 22-day old rats under control conditions were significantly higher than in adults. Desmopressin stimulated significant increase of this parameter in 22-day old pups (Pf = = 125 +/- 4.85; Pf = 174 +/- 8.2 microns/s, p < 0.001) and adult rats (Pf = 100.5 +/- 7.38; Pf = 178.8 +/- 9.54 microns/s, p < 0.001). Osmotic water permeability of the OMCD basolateral membrane in 10-day old rats does not depend on dDAVP (Pf = 172.5 +/- 23.8; Pf = 164.8 +/- 34 microns/s). With the RT-PCR, we observed a gradual increase of AQP2 and V2 receptor genes expression during postnatal ontogenesis. The gene expression of AQP3 and AQP4 remained unchanged during postnatal ontogenesis. In general, the water permeability of the OMCD basolateral membrane of rats can be stimulated by AVP since the 22nd day of postnatal life. The water permeability of the OMCD basolateral membrane under control conditions gradually decreased during postnatal development, while gene expression of AQP3 and AQP4 was unchanged. The mechanism of this decrease remains to be established.

Aging↗
PubMedDate not supplied

Effect of bur cutting patterns and dentin bonding agents on dentin permeability in a fluid flow model.

This study investigated the effects of bur cutting surface roughness and bonding systems on dentin permeability. A conventional straight edged bur, cross-cut serrated bur and an extensively serrated bur were utilized with two different bonding systems. Null hypothesis was that increased surface roughness does not decrease the permeability of dentin sealing after application of bonding agents. This study incorporated a fluid flow model for measuring dentin permeability. Seventy caries-free extracted molars were used and sectioned 2 mm apical to the cementoenamel junction (CEJ). The pulp tissue was removed and the chamber cleaned using 37% phosphoric acid followed by 1:1 sodium hypochlorite solution. The specimens were mounted to plexiglass plates using cyanoacrylate cement. A flow system was established through the pulp chamber and gravity pressurized phosphate buffered saline (PBS) was forced into the chamber and the "closed system" permeability measured. Burs were used to prepare flat surfaces in dentin, and after etching with phosphoric acid, the "open tubule" permeability was determined. After applying the dentin bonding agents, fluid flow from the pulp chamber into dentin was again measured. The percentage of reduction in permeability following bonding agent application was then calculated. A two-way ANOVA found a significant (p<0.05) decrease in bonded dentin permeability in specimens prepared using the cross-cut serrated and extensively serrated bur as compared to the conventional straight-edged bur. No significant differences were detected between bonding systems and no combination of surface topography or bonding agent completely sealed the surface.

Analysis of Variance↗
PubMed2005

Effect of Helicobacter pylori and eradication therapy on gastrointestinal permeability. Implications for patients with seronegative spondyloarthritis.

OBJECTIVE: Disruption of intestinal barrier function, followed by increased antigen load, may possibly trigger joint inflammation. In seronegative spondyloarthritis (SpA) both gut inflammation and altered intestinal permeability have been reported. We evaluated the influence of Helicobacter pylori and nonsteroidal antiinflammatory drugs (NSAID) on gastrointestinal (GI) permeability in SpA. Twenty SpA patients (7 women, mean age 47 +/- 13 SD yrs), 30 patients with endoscopic gastritis (EndG; 17 women, mean age 48 +/- 14 yrs), and 35 healthy controls (16 women, mean age 40 +/- 15 yrs) were studied. No patient was undergoing antisecretory therapy. In the SpA group, 8 patients were chronically taking NSAID and 12 took NSAID occasionally, none during the month before the study. All subjects were assessed for gastroduodenal (sucrose) and intestinal (lactulose/mannitol) permeability test and H. pylori status (urea breath test). RESULTS: H. pylori affected GI permeability in both SpA and EndG patients. After eradication therapy, sucrose excretion remained increased in SpA and reverted to normal in EndG patients, whereas lactulose/mannitol test became comparable to controls in both groups. SpA patients taking chronic NSAID had increased gastroduodenal permeability only when H. pylori-positive. In SpA patients, GI permeability did not correlate with clinical activity or biochemical inflammation. CONCLUSION: In SpA, H. pylori and NSAID contribute to impaired GI permeability. Eradication therapy may help to maintain epithelial barrier function and possibly influence clinical improvement in patients with SpA.

Adult↗
PubMed2005

Regional permeability of coenzyme Q10 in isolated rat gastrointestinal tracts.

The objective of the study was to identify the region with the maximum permeability for low bioavailable coenzyme Q10 (CoQ) in the gastrointestinal tract. To evaluate the regional differences in permeability, male Sprague-Dawley rats, 250-300 g, were anesthetized and the gastrointestinal segments were isolated. Stomach, duodenum, jejunum, ileum and colon tissues were mounted on a Navicyte side-by-side diffusion apparatus. Radiolabeled CoQ (1 microM in DMEM, pH 7.4, 37 degrees C was added to the donor side and the samples withdrawn from the receiver compartment at predetermined time intervals were analyzed using a scintillation counter. Membrane integrity was monitored by 14C-mannitol permeability. The apical to basal permeability coefficients (Papp x 10(-6), cm/s) were 0.32 +/- 0.13, 3.14 +/- 0.89, 1.36 +/- 1.4, 0.83 +/- 0.40, and 1.59 +/- 0.13, for CoQ through rat stomach, duodenum, jejunum, ileum, and colon tissues respectively. The basolateral to apical permeability coefficients (Papp x 10(-6), cm/s) were 1.6 +/- 0.2, 2.2 +/- 1.2, 0.88 +/- 0.12, 1.6 +/- 0.42, and 1.9 +/- 0.41 respectively. Therefore the region of maximum CoQ permeability is duodenum followed by colon and ileum. Jejunum and stomach regions also have fairly high permeability. Therefore CoQ formulations should be made with an aim to target the duodenum to get maximum dosage effect.

Algorithms↗